Originariamente Scritto da menphisdaemon
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Bè, ci sono atleti che vivevano per il pump... Sul fatto che il pump favorisca la cresita muscolare o ipertrofia sono daccordo in maniera molto limitata: aiuta l'afflusso degli aminoacidi e delle altre sostanze nutritive al muscolo, ma ai fini ipertrofici abbiamo semplice crescita sarcoplasmatica e capillarizzazione...insomma un'apporto che c'è ma è molto relativo.
Francamente mi piacerebbe che approfondiste l'unico argomento degno di nota e cioè la sorte dei prodotti di scarto dell'arginina.
Aspetto sempre gli studi sulla sua tossicità e su quella delle vitamine
Francamente mi piacerebbe che approfondiste l'unico argomento degno di nota e cioè la sorte dei prodotti di scarto dell'arginina.
Aspetto sempre gli studi sulla sua tossicità e su quella delle vitamine
Come ho scritto a Master, trattandosi evidentemente di sostanze a bassa (o forse nulla) tossicita', e' difficile trovare dei lavori che dimostrano in modo assoluto questa tossicita'.
Il PUNTO che ho sottolineato piu' volte, ma che pochi sembrano aver recepito, e' che stiamo parlando di sostanze da far assumere a persone SANE.
Quindi la soglia per dire "si la prendo" deve essere mooooolto alta.
Ci deve essere la garanzia di non farsi del male, e, per me almeno, dei solidi indizi di farmi del bene.
Comunque qualche cosa c'e' in rete, te ne posto alcuni, per gli altri sei il benvenuto a usare un po' del TUO tempo col culo sulla sedie davanti al pc. PubMed e' accessibile a tutti
Imunobiology. 2007;212(9-10):795-812. Epub 2007 Nov 14.
LinksRole of arginine metabolism in immunity and immunopathology.
Peranzoni E, Marigo I, Dolcetti L, Ugel S, Sonda N, Taschin E, Mantelli B, Bronte V, Zanovello P.
Department of Oncology and Surgical Sciences, Padova University, via Gattamelata 64, 35128, Padova, Italy.
A heterogeneous set of cells that are commonly grouped as "myeloid cells", interacts in a complex landscape of physiological and pathological situations. In this review we attempt to trace a profile of the "myeloid connection" through different normal and pathological states, by analyzing common metabolic pathways of the amino acid l-arginine. Myeloid cells exert various, often divergent, actions on the immune response through mechanisms that exploit mediators of this peculiar metabolic pathway, ranging from l-arginine itself to its downstream metabolites, like nitric oxide and polyamines. Various pathological situations, including neoplastic and autoimmune diseases, as well as injury repair and infections are discussed here, showing how l-arginine metabolism is able to play a dual role, both as an active protector and a possible threat to the organism.
QUESTO DICE CHE LA VIT C NON SERVE
Mech Ageing Dev. 2006 Dec;127(12):897-904. Epub 2006 Nov 7.
LinksLife-long vitamin C supplementation in combination with cold exposure does not affect oxidative damage or lifespan in mice, but decreases expression of antioxidant protection genes.
Selman C, McLaren JS, Meyer C, Duncan JS, Redman P, Collins AR, Duthie GG, Speakman JR.
Aberdeen Centre for Energy Regulation and Obesity (ACERO), School of Biological Sciences, University of Aberdeen, Aberdeen AB24 2TZ, UK. c.selman@ucl.ac.uk
Oxidative stress is suggested to be central to the ageing process, with endogenous antioxidant defence and repair mechanisms in place to minimize damage. Theoretically, supplementation with exogenous antioxidants might support the endogenous antioxidant system, thereby reducing oxidative damage, ageing-related functional decline and prolonging life- and health-span. Yet supplementation trials with antioxidants in animal models have had minimal success. Human epidemiological data are similarly unimpressive, leading some to question whether vitamin C, for example, might have pro-oxidant properties in vivo. We supplemented cold exposed (7+/-2 degrees C) female C57BL/6 mice over their lifespan with vitamin C (ascorbyl-2-polyphosphate), widely advocated and self administered to reduce oxidative stress, retard ageing and increase healthy lifespan. No effect on mean or maximum lifespan following vitamin C treatment or any significant impact on body mass, or on parameters of energy metabolism was observed. Moreover, no differences in hepatocyte and lymphocyte DNA oxidative damage or hepatic lipid peroxidation was seen between supplemented and control mice. Using a DNA macroarray specific for oxidative stress-related genes, we found that after 18 months of supplementation, mice exhibited a significantly reduced expression of several genes in the liver linked to free-radical scavenging, including Mn-superoxide dismutase. We confirmed these effects by Northern blotting and found additional down-regulation of glutathione peroxidase (not present on macroarray) in the vitamin C treated group. We suggest that high dietary doses of vitamin C are ineffective at prolonging lifespan in mice because any positive benefits derived as an antioxidant are offset by compensatory reductions in endogenous protection mechanisms, leading to no net reduction in accumulated oxidative damage.
QUI DESCRIVONO UN CASO IN CUI L'ECCESSO DI VIT C, INSIEME AD ALTRI SUPPLEMENTI, HA PROBABILMENTE CAUSATO UN DANNO RENALE.
Clin Nephrol. 2005 Sep;64(3):236-40. Links
Supplement nephropathy due to long-term, high-dose ingestion of ascorbic acid, calcium lactate, vitamin D and laxatives.
Ohtake T, Kobayashi S, Negishi K, Moriya H.
Department of Nephrology, and Kidney and Dialysis Center, Shonan Kamakura General Hospital, Yamazaki, Kamakura, Japan. ohtake@shonankamakura.or.jp
A 48-year-old Japanese woman previously in good health was found to have severe proximal tubular dysfunction with a high serum level of ascorbic acid (57.3 microg/ml, reference range: 1.9 - 15.0 microg/ml). Renal biopsy specimen showed marked tubulointerstitial damage, i.e. tubular atrophy, dilatation of tubular lumen with flattened tubular epithelial cells, vacuolization of proximal and distal tubular epithelial cells, and severe interstitial fibrosis with mild infiltration of mononuclear cells. Calcified lesions, which caused tubular obstruction or stenosis, were also seen in interstitial area adjacent to degenerated proximal tubuli. Hypokalemic nephropathy, probably due to long-term use of laxatives, was clearly shown. However, calcified lesions seemed to be caused by inappropriate excessive daily ingestion of ascorbic acid (6 000 mg/day), calcium lactate, and vitamin D because of the patient's misunderstanding that these supplements could keep her in a good health. This condition may be clinically called "supplement nephropathy".
QUI DICE CHE NON SERVE COME ANTIOSSIDANTE (NELLE DOSI TESTATE)
Eur J Nutr. 2006 Mar;45(2):97-104. Epub 2005 Jul 18.
LinksDietary supplementation with different vitamin C doses: no effect on oxidative DNA damage in healthy people.
Herbert KE, Fletcher S, Chauhan D, Ladapo A, Nirwan J, Munson S, Mistry P.
Dept. of Cardiovascular Sciences, University of Leicester Robert Kilpatrick Building, Leicester Royal Infirmary, Leicester LE2 7LX, UK.
BACKGROUND: Antioxidants are believed to prevent many types of disease. Some previous studies suggest that dietary supplementation with vitamin C results in a decrease in the level of one of the markers of oxidative damage-8-oxoguanine in the DNA of peripheral blood mononuclear cells (PBMC). AIM OF TRIAL: To investigate the effect of different dose levels of dietary supplementation with vitamin C on oxidative DNA damage. METHODS: A randomised double-blind placebo-controlled trial was carried out using three different levels (80, 200 and 400 mg) of dietary vitamin C supplementation in a healthy population of 160 volunteers; supplementation was for a period of 15 weeks followed by a 10 week washout period. Peripheral blood samples were obtained every 5 weeks from baseline to 25 weeks. RESULTS: An increase in PBMC vitamin C levels was not observed following supplementation in healthy volunteers. There was no effect found on 8-oxoguanine measured using HPLC with electrochemical detection for any of the three supplemented groups compared to placebo. 8-oxoadenine levels were below the limit of detection of the HPLC system used here. CONCLUSIONS: Supplementation with vitamin C had little effect on cellular levels in this group of healthy individuals, suggesting their diets were replete in vitamin C. The dose range of vitamin C used did not affect oxidative damage in PBMC DNA.
QUESTO SAREBBE DA LEGGERE NEL DETTAGLIO; PERCHE' CITA "INCREASE IN SPECIFIC BASE LESIONS"
Free Radic Res. 2005 Jul;39(7):671-86.
LinksReview: When is an antioxidant not an antioxidant? A review of novel actions and reactions of vitamin C.
Duarte TL, Lunec J.
Pharmaceutical Sciences Research Division, Kings College London University.
Vitamin C (or ascorbic acid) is regarded as the most important water-soluble antioxidant in human plasma and mammalian cells which have mechanisms to recycle and accumulate it against a concentration gradient, suggesting that the vitamin might also have important intracellular functions. In this review we summarize evidence from human trials that have attempted an association between vitamin C supplementation and an effect on biomarkers of oxidative DNA damage. Most studies reviewed herein showed either a vitamin C-mediated reduction in oxidative DNA damage or a null effect, whereas only a few studies showed an increase in specific base lesions. We also address the possible beneficial effects of vitamin C supplementation for the prevention of cancer and cardiovascular disease. Finally, we discuss the contribution of cell culture studies to our understanding of the mode of action of vitamin C and we review recent evidence that vitamin C is able to modulate gene expression and cellular function, with a particular interest in cell differentiation.
QUI' NOTANO UN EFFETTO PROMOTORE DELLA VIT C NEL CANCRO DELL'ESOFAGO (DELLE CAVIE) QUANDO PRESENTI NITRATI DI SODIO (che presenti in numerosi insaccati come conservanti) E REFLUSSO .
Cancer Sci. 2008 Jan;99(1):7-13. Epub 2007 Oct 22.
LinksEnhancement of esophageal carcinogenesis in acid reflux model rats treated with ascorbic acid and sodium nitrite in combination with or without initiation.
Kuroiwa Y, Okamura T, Ishii Y, Umemura T, Tasaki M, Kanki K, Mitsumori K, Hirose M, Nishikawa A.
Division of Pathology, National Institute of Health Sciences, 1-18-1 Kamiyoga, Setagaya-Ku, Tokyo 158-8501, Japan.
Combined treatment with sodium nitrite (NaNO2) and ascorbic acid (AsA) has already been shown to promote rat forestomach carcinogenesis, possibly due to nitric oxide generation under acidic conditions. We hypothesized that a similar effect might occur in the esophagus when the luminal pH is decreased by acid reflux. To clarify this possibility, reflux esophagitis model rats (F344 male) were coadministered 0.2% NaNO2 in the drinking water and 1% AsA in the diet. After 32 weeks of the combined treatment, a significant increase in the incidence of epithelial hyperplasias of the lower-middle and lowest parts of the esophagus were observed compared with the basal-diet group, along with exacerbation of dysplasia and extension of the lesions. Additionally, one squamous cell papilloma was found only in the combined-treatment group. Subsequently, we confirmed the enhancing effects of NaNO2 and AsA cotreatment in the rat N-bis(2-hydroxypropyl)nitrosamine-initiated esophageal tumorigenesis model. The incidence of hyperplasia was enhanced in all segments, along with the incidence and multiplicity of squamous cell papillomas in the lowest segment of the esophagus. Thus, the data demonstrate that combined treatment with NaNO2 and AsA exerts promoting effects on rat esophageal carcinogenesis under acid reflux conditions, as in the forestomach. These findings suggest that the risk of excessive intake of a combination of nitrite and antioxidants for esophageal carcinogenesis is appreciable, particularly in patients with reflux esophagitis.
QUI PARLANO DI COME I DANNI DA NO SIANO IN REALTA' DOVUTI AD UN COMPOSTO DERIVATO ...
Physiol Rev. 2007 Jan;87(1):315-424.
LinksNitric oxide and peroxynitrite in health and disease.
Pacher P, Beckman JS, Liaudet L.
Section on Oxidative Stress Tissue Injury, Laboratory of Physiologic Studies, National Institutes of Health, National Institute of Alcohol Abuse and Alcoholism, Bethesda, Maryland, USA. pacher@mail.nih.gov
The discovery that mammalian cells have the ability to synthesize the free radical nitric oxide (NO) has stimulated an extraordinary impetus for scientific research in all the fields of biology and medicine. Since its early description as an endothelial-derived relaxing factor, NO has emerged as a fundamental signaling device regulating virtually every critical cellular function, as well as a potent mediator of cellular damage in a wide range of conditions. Recent evidence indicates that most of the cytotoxicity attributed to NO is rather due to peroxynitrite, produced from the diffusion-controlled reaction between NO and another free radical, the superoxide anion. Peroxynitrite interacts with lipids, DNA, and proteins via direct oxidative reactions or via indirect, radical-mediated mechanisms. These reactions trigger cellular responses ranging from subtle modulations of cell signaling to overwhelming oxidative injury, committing cells to necrosis or apoptosis. In vivo, peroxynitrite generation represents a crucial pathogenic mechanism in conditions such as stroke, myocardial infarction, chronic heart failure, diabetes, circulatory shock, chronic inflammatory diseases, cancer, and neurodegenerative disorders. Hence, novel pharmacological strategies aimed at removing peroxynitrite might represent powerful therapeutic tools in the future. Evidence supporting these novel roles of NO and peroxynitrite is presented in detail in this review.
, come volessi dire "se non ci sono gli studi, e senza che si scriva - potrebbe - voglio delle certezze" ... e poi posti delle opinioni tue personalissime mettendo addirittura le % ... mah ... 
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